For decades it didn’t look like clioquinol was going to qualify for the Pharmaceuticals Hall of Fame.

The hydroxyquinoline antibiotic had been used since World War II to treat amoebic infections and shigella gastroenteritis until being blamed for an enormous outbreak of subacute myelo-optic neuropathy in Japan in the 1960s.

There was little scientific reasoning behind the presumed association, and the drug had been used safely by millions before the epidemic but hey, other antibiotics were available to treat the conditions in question so why take a chance?

So the drug passed quietly into retirement, presumably never to be heard from again.

But then out of nowhere, recent animal studies have surfaced purporting to show that clioquinol reverses progression of not one but 3 seemingly unrelated neurodegenerative conditions–Alzheimer’s, Huntington’s and Parkinson’s disease, respectively.

That’s got to be the greatest comeback since Cream rocked Madison Square Garden in 2005.

“The drug affects a gene which when inhibited can slow down aging,” Siegfried Hekimi told the Journal of Life Sciences. “The implication is that we can change the rate of aging. This might be why clioquinol is able to work on this diversity of diseases that are all age-dependent.”

Hekimi and colleagues at McGill University recently reported in the Journal of Biological Chemistry that clioquinol inhibits a mitochondrial enzyme known as CLK-1, or simply “clock-1.”

The mechanism by which clioquinol inhibits CLK-1 remains unclear. “One possibility is that metals are involved as clioquinol is a metal chelator,” Hekimi explained.